Research Focus

My intellectual and professional development has been shaped by a desire to discover and elucidate physiological and pathological processes involved in human diseases, especially the upper and lower airways, to generate potentially new therapeutic approaches to disease.

Practicing as an ENT physician after graduating from Tongji Medical University, China, my interests gradually focused on Rhinology. Although Rhinology is a branch of otolaryngology, nose and nasal sinus diseases should be considered in part to be airway diseases since they are very similar in epithelial cell phenotype, defense mechanisms, and pathophysiology. Hence, for the last several years, I have been working as a Postdoctoral Research Associate and Research Associate currently, in CW Davis' Lab in the UNC Cystic Fibrosis Center.

The goal of my work has been to understand the molecular mechanism of mucin secretion. Mucins are secreted from goblet cells and submucosal glands; after that, they mature into mucus, a key component in mucocialiary clearance. An experimental mouse trachea perfusion system was established, and multiple strains of gene-manipulated mice were studied.

In our most significant work, we found that the exocytotic priming protein, Munc13-2 mediates basal mucin secretion. This work was conducted in the mouse airways, where the principal secretory cell, the Clara cell, was previously considered a non-mucin secreting cell type under control conditions. In the Munc13-2 null mouse, we observed significant mucin stores. Significantly, these findings may indicate that human Clara cells are the source of mucins in the small airways, the site where airway diseases such as chronic bronchitis and cystic fibrosis are thought to be initiated. Hence, our work indicates that the mucin basal secretory pathway may play an important role in airway physiology and pathology.

In the present, I am focusing on studying the molecular mechanism and regulation of basal mucin secretion and of mechanical stimulation induced mucin secretion.

Project: MARCKS (myristoylated alanine-rich C kinase substrate) regulates degranulation of mast cells and mucin secretion of airway goblet cells.Result: Although MARCKS is one of the PKC substrates, it is not essential for either degranulation of mast cells, or mucin secretion of airway goblet cells.

Dissertation Completion Fellowship from Graduate school, Michigan State University during Summer, 2009.

Junior Investigator Travel Fellowship from The New York Academy of Sciences to attend “Hypoxia and Consequences: From Molecule and Malady” meeting, The New York Academy of Sciences, 2009 at New York, USA.

Student/Postdoctoral-Young Investigator Merit Award by Association of Scientists of Indian Origin (ASIO) at Society of Toxicology Conference, 2009 at Baltimore, USA.

Qualified national level CSIR (Council for Scientific and Industrial Research)-Human Resource Development Group Junior Research Fellowship (JRF) for PhD (2002-2003) held on 23rd June 2002.

Qualified national level National Eligibility Test (NET) for Lectureship conducted by CSIR-UGC held on 22nd December 2002.

Qualified national level National Eligibility Test (NET) for Lectureship conducted by Indian Council for Agricultural Research (ICAR).

Awarded fellowship as Junior Research Fellowship (JRF) under Department of Biotechnology (DBT), New Delhi, sponsored project entitled “Development of PCR based assay for molecular diagnosis of Chlamydia psittaci”.